title: Hypertension in kidney transplant recipients.
abstract: Arterial hypertension is frequently observed in renal transplant recipients. Its pathogenesis is multifactorial in most cases. Calcineurin inhibitors (CNI) can increase peripheral vascular resistance by inducing arteriolar vasoconstriction and can cause extracellular fluid expansion by reducing the glomerular filtration rate (GFR), activating the renin-angiotensin system (RAS), and by inactivating the atrial natriuretic peptide. Glucocorticoids can impair urinary water and salt excretion. Poor graft function can lead to increased extracellular volume and inappropriate production of renin. Native kidneys, older age of the donor and transplant renal artery stenosis (TRAS) may also contribute to the development of hypertension. Arterial hypertension not only can increases the risk for cardiovascular events but can also deteriorate renal allograft function. A number of studies have shown that the higher the levels of blood pressure are, the higher is the risk of graft failure. On the other hand, a good control of blood pressure may prevent many cardiovascular and renal complications. Appropriate lifestyle modification is the first step for treating hypertension. Calcium channel blockers (CCB) and renin-angiotensin system (RAS) inhibitors are the most frequently used antihypertensive agents, but in many cases, a combination of these and other drugs is required to obtain good control of hypertension.
authors.affiliation: Nephrology and Dialysis Unit, Istituto Clinico Humanitas, IRCCS, Via Manzoni 56, Rozzano-Milano, Italy. claudio.ponticelli@fastwebnet.it
authors.forename: Claudio
authors.initials: C
authors.lastname: Ponticelli
authors.forename: David
authors.initials: D
authors.lastname: Cucchiari
authors.forename: Giorgio
authors.initials: G
authors.lastname: Graziani
mesh_terms: D000317:Adrenergic alpha-Antagonists / Q000627:therapeutic use; D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000804:Angiotensin II / Q000502:physiology; D057911:Angiotensin Receptor Antagonists / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D065095:Calcineurin Inhibitors; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D002318:Cardiovascular Diseases / Q000209:etiology; D016572:Cyclosporine / Q000009:adverse effects; D004232:Diuretics / Q000627:therapeutic use; D005938:Glucocorticoids / Q000009:adverse effects; D006084:Graft Rejection / Q000209:etiology; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000188:drug therapy / Q000209:etiology*; D007166:Immunosuppressive Agents / Q000009:adverse effects; D016030:Kidney Transplantation / Q000009:adverse effects*; D008019:Life Style; D012078:Renal Artery Obstruction / Q000150:complications; D014655:Vascular Resistance / Q000187:drug effects
chemical_list: D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D065095:Calcineurin Inhibitors; D002121:Calcium Channel Blockers; D004232:Diuretics; D005938:Glucocorticoids; D007166:Immunosuppressive Agents; D000804:Angiotensin II; D016572:Cyclosporine